Pathogenic mechanisms for preeclampsia include end organ vasoconstriction, platelet aggregation, and reduced trophoblastic invasion of the uterine spinal arteries. This protocol aims to focus on activation of platelets in the pathogensis of preeclampsia by evaluating the levels of expression of P-selectin, CD 63, PAC platelet antigens and fibrinogen receptors in the whole blood of preeclamptic and control patients. Flow cytometry and monoclonal antibodies will be utilized. The etiology of platelet activation is most likely due to the placenta and will be evaluated by trophoblasts cultured under hypoxic conditions. Markers of platelet activation as above will be measured in trophoblastic cultured cells. Modulation of platelet activation as regulated by guanine nucleotide-binding proteins will be evaluated. The preeclamptic patients' blood will be obtained from blood that was banked in Protocol #733. The data base and statistical analysis provided by the GCRC will again be utilized. The core lab will be utilized for blood separation and laminar flow hoods.